Babesiosis, like malaria, is a disease which has a focal character. The reason for this is that the pathogen is transmitted by ticks that feed on a certain reservoir of parasites present in the vertebrate population. Only where ticks are present, babesiosis can occur. On balance, particularly in indigenous animals, the parasite coexists with the host without causing significant disease. In many cases babesiosis is a problem because of man's activities through inbreeding of genetic traits and/or transporting animals to unfamiliar environments where babesiosis is endemic (Callow, L. L and Dalgliesh, R. J., 1982).
In dogs the disease is caused by B. canis (transmitted by Dermacentor ticks), B. rossi (transmitted by Haemaphysalis ticks), B. vogeli (transmitted by Rhipicephalus ticks) and Babesia gibsoni (transmitted by Haemaphysalis and Rhipicephalus ticks). Signs of disease in naturally acquired babesiosis usually begin 7–21 days after infection. These symptoms include: fever, anorexia, depression, anaemia, haemoglobinuria and rapidly developing weakness. Increased lacrimation, salivation and muscle tremor commonly occur. Nervous signs may develop in terminal infections, and death may occur when the disease is left untreated. Severe coagulation disturbances resembling disseminated intravascular coagulation (DIC) have been reported in acute B. canis infections. Thrombosis is not common, but small hyaline thrombi, connected with megakaryocytes have been described. It appears that these coagulation disturbances lead to increased erythrocyte-stickiness. As a result the blood passage through the microvasculature is hampered, resulting in congestion of internal organs and decreased packed cell volumes (PCV). This might impair the oxygen supply to certain tissues and subsequently lead to tissue damage as a result of anoxia. Evidence from congestion in B. canis infections comes from experiments in which dogs were chemotherapeutically treated. Some of these animals restore the packed cell volume in two days from 25–35%, which is associated with shrinkage of the spleen to normal measures.
The four species of Babesia differ with respect to their pathogenicity. The North-African B. vogeli strains provoke only mild disease, which usually does not require treatment (like the Australian B. canis strains). European B. canis strains are more pathogenic than the North-African parasite. In our experiments with the B. canis A strain, approximately half of the animals required chemotherapeutic treatment after infection. The South-African B. rossi strains are most pathogenic, a feature observed already very early. Using the South-African B. rossi strain naive dogs developed progressing disease characterised by exponential parasite growth. In contrast, parasitaemia in dogs infected with European B. canis usually is limited. In the latter, congestion appears to be the main pathological feature.
At the moment a vaccine for Babesia is prepared from the supernatant of a culture of a strain of Babesia canis, as is described in U.S. Pat. No. 4,777,036. However, such a vaccine contains only antigens of the strain of this particular species of B. canis. It appears that such a vaccine gives in general little protection against infections with (wild type) B. canis (Lepetit, C., Piroplasmose canine et vaccination Pirodog, Doctoral Thesis, Univ. of Nantes, 1988). The author of the thesis gives three possible causes of this failure of protective immunisation:    1. the sensitivity of the dogs with respect to vaccination;    2. the type of immune effector mechanism induced by vaccination;    3. the antigenic diversity of Babesia. 
Vaccines containing whole, attenuated Babesia parasites always harbour the danger that the parasites again become virulent and thus spread the disease instead of curing it. Therefore, the use of subunit vaccines is preferred. Thus there remains the desire for a vaccine which is not infective, which can be easily produced and which yet can give protection against Babesia canis infection, preferably against all Babesia canis strains.